Morphometric analysis of the composition of coronary arterial plaques in isolated unstable angina pectoris with pain at rest

Coronary artery plaque morphology was studied in 354 five-mm segments of the 4 major (left main, left anterior descending, left circumflex and right) epicardial coronary arteries in 10 patients with isolated unstable angina pectoris with pain at rest. The 4 major coronary arteries were sectioned at 5-mm intervals and a drawing of each of the resulting 354 Movat-stained histologic sections was analyzed using a computerized morphometry system. The major component of plaque was a combination of dense acellular and cellular fibrous tissue with much smaller portions of plaque being composed of pultaceous debris, calcium, foam cells with and without inflammatory infiltrates and inflammatory infiltrates without foam cells. There were no differences in plaque composition among any of the 4 major epicardial coronary arteries. Plaque composition varied as a function of the degree of luminal narrowing. Linear increases were observed in the mean percent of dense fibrous tissue (from 5 to 50%), calcific deposits (from 1 to 10%), pultaceous debris (from 0 to 10%) and inflammatory infiltrates without significant numbers of foam cells (from 0 to 5%), and a linear decrease was observed in the mean percent of cellular fibrous tissue (from 94 to 22%) in sections narrowed up to 25% to more than 95% in cross-sectional area. Multiluminal channels were seen in all 10 patients (28 [19%] of the 146 sections narrowed greater than 75% in cross-sectional area and in 36 [10%] of all 354 segments); occlusive thrombi in no patient; nonocclusive thrombi in 2 patients (1 section each of 2 arteries); plaque rupture in 2 patients (4 segments from 2 arteries); and plaque hemorrhages in 6 patients (11 sections from 10 arteries).     

Sudden coronary death: comparison of patients with to those without coronary thrombus at necropsy

Among 70 victims of sudden coronary death (SCD), certain clinical and morphologic findings in the 13 with a coronary thrombus are compared with the findings in 57 victims without a coronary thrombus. The 13 with a thrombus were younger than those without (mean age 43 vs 51 years, p less than 0.02); had a lower mean percent of cross-sectional area (XSA) narrowing by plaque at the site of maximal coronary stenosis (89% vs 95%, p less than 0.01); and had a higher mean percent of 5-mm segments of the 4 major epicardial coronary arteries minimally narrowed (0 to 25% in XSA) by plaque (27% vs 19%, p less than 0.001). No differences occurred in the 2 groups with regard to sex, previous angina pectoris or clinical acute myocardial infarction, healed myocardial infarction at necropsy, mean heart weight, number of major coronary arteries narrowed 76 to 100% in XSA by atherosclerotic plaque, or the mean percent of 5-mm segments of the 4 major epicardial coronary arteries narrowed 76 to 100% in XSA by atherosclerotic plaque. Thus, coronary thrombi are infrequent in victims of SCD, and when observed, their significance is uncertain because victims of SCD without coronary thrombi have similar amounts of severe coronary narrowing.     

Composition of atherosclerotic plaques in the four major epicardial coronary arteries in patients greater than or equal to 90 years of age

The composition of atherosclerotic plaques in 733 five-mm segments of the 4 major (left main, left anterior descending, left circumflex and right) epicardial coronary arteries of 18 patients greater than or equal to 90 years of age was determined by computerized planimetric analysis. By analysis of all coronary segments of all patients greater than 90, the plaques consisted primarily of fibrous tissue (87 +/- 8%) with calcific deposits (7 +/- 6%), pultaceous debris (5 +/- 4%) and foam cells (1 +/- 1%) occupying a much smaller percentage of plaque area. Analysis of composition according to the 4 degrees of luminal cross-sectional area narrowing revealed marked step-wise increases in pultaceous debris (from 0 +/- 0% at 0 to 25% narrowing to 18 +/- 22% at 76 to 100% narrowing, p = 0.0001) and calcific deposits (from 0 +/- 0 to 10 +/- 15%, p = 0.002), and decreases in fibrous tissue (from 99 +/- 3 to 71 +/- 23%, p = 0.0001) and area occupied by the media (from 35 +/- 8 to 16 +/- 8%, p = 0.0001). When the analysis was restricted to sections narrowed greater than 75%, no significant differences were found in plaque components or medial area between patients with (11 patients) and without (7 patients) myocardial infarcts at necropsy.     

Composition of atherosclerotic plaques in the epicardial coronary arteries in juvenile (type I) diabetes mellitus.

The composition of atherosclerotic plaques in 331 five-mm segments of the 4 major (left main, left anterior descending, left circumflex, and right) epicardial coronary arteries of 8 patients with juvenile (mean age at onset, 9 years; mean age at death, 29 years) diabetes mellitus was determined by computerized planimetric analysis. Analysis of all coronary segments disclosed that the plaques consisted primarily of dense (53%) and cellular (38%) fibrous tissue. Pultaceous debris (7%), foam cells (1.2%) and calcific deposits (0.7%) occupied a small percentage of the plaques. Thus, 91% of the coronary plaques in these young diabetic patients consisted of fibrous tissue and nearly all of the remaining 9% consisted of lipid deposits. Analysis of composition according to degrees of cross-sectional luminal narrowing revealed marked increases in dense fibrous tissue (from 31 to 74%), pultaceous debris (from 3 to 12%), and calcific deposits (from 0% to 3%) as the cross-sectional area narrowing increased from < or = 25% to > 75%. Compared with older patients with fatal coronary artery disease, the patients with juvenile diabetes had more dense fibrous tissue and pultaceous debris and less calcific deposits.     

Composition of atherosclerotic plaques in coronary arteries in women less than 40 years of age with fatal coronary artery disease and implications for plaque reversibility

This study analyzes the composition of atherosclerotic plaques in the 4 major epicardial coronary arteries in 8 women less than 40 years of age (mean 34) with fatal coronary artery disease (CAD) and compares these data to previous studies of 37 adults greater than 45 years of age (mean 59) with fatal CAD. Histologic sections were taken at 5-mm intervals from the entire lengths of the right, left main, left anterior descending and left circumflex coronary arteries. With the use of a computerized morphometry system, analysis of the 4 major epicardial coronary arteries showed the major component of plaque to be a combination of cellular (mean percent total plaque area = 65%, standard error = 6%) and dense (19%, standard error = 6%) fibrous tissue. Arterial segments narrowed greater than 75% in cross-sectional area from these young women were compared with similarly narrowed arteries from 37 older patients (32 men [86%]) with fatal CAD previously reported by this laboratory, and showed significantly more cellular fibrous tissue and lipid-rich foam cells, and lesser amounts of dense fibrous and heavily calcified tissue. The large amount of lipid-containing foam cells and relative lack of acellular scar tissue in coronary plaques in these young women suggests a greater potential for reversibility of these plaques in this subset of patients with CAD.     

Diffuse extent of coronary atherosclerosis in fatal coronary artery disease

In 4 subsets of patients with coronary artery disease, the amounts of narrowing of the 4 major epicardial coronary arteries were compared (left main, left anterior descending, left circumflex and right) by atherosclerotic plaques. Among 129 patients studied at necropsy, an average of 2.7 of the 4 arteries were narrowed greater than 75% in cross-sectional area at some point; in control subjects, narrowing was seen in an average of 0.7 arteries. Patients with unstable angina pectoris had a greater incidence of narrowing (3.2 arteries) than did patients with sudden coronary death (2.8), acute myocardial infarction (MI) (2.7) or healed MI (2.3). Each of the 4 major arteries was divided into segments 5 mm in length, and histologic sections were prepared and stained by the Movat method. A total of 6,461 segments were analyzed from the 129 patients and 1,849 from the 40 controls. In the 129 patients, 35% of the 5-mm segments were narrowed 75 to 100% in cross-sectional area (compared with 3% in control subjects). The group with unstable angina had the highest percentage (48%) of severely narrowed segments compared with the groups with sudden coronary death (36%), acute (34%) and healed MI (31%). Only 8% of the 6,461 segments were narrowed less than or equal to 25% in cross-sectional area, and virtually none of the 6,461 segments was normal; thus, 92% of the coronary segments were narrowed greater than 25% in cross-sectional area by atherosclerotic plaque alone. Among patients with fatal coronary artery disease studied at necropsy, therefore, the atherosclerotic process is severe and diffuse in the major epicardial coronary arteries.     

Severe atherosclerotic coronary arterial narrowing and chronic congestive heart failure without myocardial infarction: analysis of 18 patients studied at necropsy

Observations are reported on 18 patients (aged 38 to 73 years ([mean 58]; 16 [89%] men) studied at necropsy who had had chronic congestive heart failure (CHF) more than 3 months in duration, greater than 75% cross-sectional area (XSA) narrowing of 1 or more of the 4 major epicardial coronary arteries, and no left ventricular fibrosis or necrosis. Duration of symptoms from onset of CHF to death ranged from 0.3 to 13 years (mean 5.7). Angina pectoris occurred in 2 patients (11%). The mode of death was CHF in 12 (67%), sudden (arrhythmia) in 5 (28%), and emboli in 1 (5%). Heart weight ranged from 410 to 890 g (mean 632). Of 72 major epicardial coronary arteries (right, left main, left anterior descending, left circumflex) in the 18 patients, 30 (42%) were narrowed 76 to 100% in XSA by atherosclerotic plaque (right = 10, left main = 0, left anterior descending = 9 and left circumflex = 11). A mean of 1.7 of 4 major epicardial coronary arteries per patient were narrowed 76 to 100% in XSA by atherosclerotic plaque. In 10 patients, each 5-mm segment of the 4 major coronary arteries was examined histologically (mean 53 per patient): 23 segments (3%) were narrowed 96 to 100% in XSA by atherosclerotic plaque; 58 (11%), 76 to 95; 93 (18%), 51 to 75%; 209 (40%), 26 to 50%, and 146 (28%), 0 to 25%. Left and right ventricular thrombi were found in 9 patients (50%); of the 9 patients, 1 had a systemic embolus; of the 9 patients without intraventricular thrombi, none had systemic emboli.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sudden coronary death

Many reports have described the amounts of atherosclerotic plaque in victims of sudden coronary death, defining the number of coronary arteries narrowed at some point greater than 75% in cross-sectional area (XSA). In order to quantitate more precisely the amount and distribution of plaque, 70 victims of sudden coronary death aged 22-81 years (mean 50) were studied. The four major epicardial coronary arteries (left main, left anterior descending, left circumflex, and right) from each of 70 victims were cut into 5-mm segments (average 50 per patient) and a histologic section prepared from each segment. The amount of luminal narrowing by plaque was categorized into five groups (0-25%, 26-50%, 51-75%, 76-95%, 96-100%). Of 3,484 five-mm segments, 950 (27%) were narrowed 76-100% in XSA. Comparison of 31 previously symptomatic victims (angina pectoris and/or myocardial infarction) to 39 victims who had been asymptomatic disclosed a higher mean percent of severely narrowed segments (30% vs. 25%, p = less than 0.005) and a lower mean percent of minimally narrowed segments in the symptomatic group. Comparison of the 31 patients with a healed myocardial infarction at necropsy with 39 patients with no left ventricular scar disclosed a higher mean percent of segments severely narrowed (33% vs. 24%, p = less than 0.001) and a lower mean percent of segments narrowed minimally in those with a left ventricular scar (13% vs. 26%, p = less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Radiation heart disease. Analysis of 16 young (aged 15 to 33 years) necropsy patients who received over 3,500 rads to the heart

Certain clinical and necropsy findings are described in 16 young (aged 15 to 33 years) patients who received greater than 3,500 rads to the heart five to 144 months before death. All 16 had some radiation-induced damage to the heart: 15 had thickened pericardia (five of whom had evidence of cardiac tamponade); eight had increased interstitial myocardial fibrosis, particularly in the right ventricle; 12 had fibrous thickening of the mural endocardium and 13 of the valvular endocardium. Except for valvular thickening, the changes were more frequent in the right side of the heart than in the left, presumably because of higher radiation doses to the anterior surface of the heart. In six of the 16 study patients and in one of 10 control subjects, one or more major epicardial coronary arteries were narrowed from 76 to 100 percent in cross-sectional area by atherosclerotic plaque; one patient had a healed myocardial infarct at necropsy and one died suddenly. In 10 patients and in the 10 control subjects, the four major epicardial coronary arteries were examined quantitatively: 6 percent of the 469 five millimeter segments of coronary artery from the patients were narrowed from 76 to 100 percent (controls = 0.2 percent, p = 0.06) and 22 percent were narrowed from 51 to 75 percent (controls = 12 percent). The proximal portion of the arteries in the patients had significantly more narrowing than the distal portions. The arterial plaques in the patients were largely composed of fibrous tissue; the media were frequently replaced by fibrous tissue, and the adventitia were often densely thickened by fibrous tissue. In five patients, there was focal thickening (with or without luminal narrowing) of the intramural coronary arteries. Thus, radiation to the heart may produce a wide spectrum of functional and anatomic changes but particularly damage to the pericardia and the underlying epicardial coronary arteries.     

Quantitative analysis of amounts of coronary arterial narrowing in cocaine addicts

From January 1979 to February 1989, 22 cocaine addicts were studied at necropsy. The 22 patients were divided into 2 groups: death associated with increased cocaine levels at necropsy (13 patients, aged 23 to 45 years [mean 32], and mean total blood cocaine level, 0.36 mg/dl) and noncocaine-related death (9 patients, aged 15 to 50 years [mean 32]). Of the 22 patients, 17 were men and 5 were women; 19 were black and 3 were white. Gross examination in the 22 patients disclosed that 8 patients (36%) had 1 or more of the 4 major (left main, left anterior descending, left circumflex, and right) coronary arteries narrowed at some point greater than 75% in cross-sectional area by atherosclerotic plaque. In 17 cases, the 4 major epicardial coronary arteries were divided into 805 five-mm long segments and a histologic section was prepared from each segment: of the 12 patients with a cocaine-related death, 41 (8%) of 544 five-mm coronary segments were narrowed 76 to 100% and 106 segments (19%) were narrowed 51 to 75% in cross-sectional area by plaque. Of the 5 cocaine addicts who did not die from cocaine overdose, 8 (3%) of 261 five-mm coronary segments were narrowed 76 to 100% and 19 segments (7%) were narrowed 51 to 75% in cross-sectional area by plaque. The frequency of coronary artery disease was greater in patients dying with cocaine in their blood at necropsy compared to those whose death was not cocaine related.(ABSTRACT TRUNCATED AT 250 WORDS)     

Rupture of the left ventricular free wall during acute myocardial infarction: analysis of 138 necropsy patients and comparison with 50 necropsy patients with acute myocardial infarction without rupture

Clinical and necropsy findings in 138 patients (69 men and 69 women) with rupture of the left ventricular (LV) free wall during acute myocardial infarction (AMI) (rupture group) were compared with 50 patients who died during their first AMI without rupture (nonrupture group). The frequency of systemic hypertension (55 vs 52%), angina pectoris (13 vs 22%) and congestive heart failure (0 vs 0%) before the fatal AMI was similar for both rupture and nonrupture groups. Mean heart weights for men (479 vs 526 g) and women (399 vs 432 g) with and without rupture also were insignificantly different. LV scar before the infarct that ruptured was present in 18 patients (13%); previous necropsy studies of fatal AMI without rupture have indicated that 50% have LV scars. The rupture group had a significantly more frequent (p less than 0.01) lateral wall location of the infarct (12 vs 2%). The number of 3 major (right, left anterior descending and left circumflex) epicardial coronary arteries narrowed at some point greater than 75% in cross-sectional area by atherosclerotic plaque was significantly lower (p less than 0.01) in the rupture group (39 vs 58%). The percent of these 3 arteries totally occluded or nearly so (greater than 95% in cross-sectional area) by plaque also was significantly less (p less than 0.001) in the rupture group (24 of 198 arteries [12%] vs 38 of 144 arteries [26%]). Analysis of each 5-mm long segment of these arteries in each group disclosed that the rupture group had significantly less narrowing than the nonrupture group. Of the 3,287 five-mm segments of artery examined in the rupture group (66 patients), 512 (15%) were narrowed greater than 75% in cross-sectional area by plaque; in contrast, of the 1,848 five-mm segments in the nonrupture group (38 patients), 508 (28%) were narrowed to this degree by plaque (p less than 0.0001). Thus, rupture of the LV free wall primarily is a complication of the first AMI and is associated with considerably less amounts of coronary narrowing than fatal AMI without rupture.     

Natural history, clinical consequences, and morphologic features of coronary arterial aneurysms in adults

Clinical and morphologic features are described in 20 adults (15 men) aged 17 to 85 years (mean 56) who at necropsy were found to have ≥1 aneurysm in ≥1 of their 3 major (right, left anterior descending, and left circumflex) epicardial coronary arteries. Of the 34 coronary aneurysms in the 20 patients (single in 10 patients, ≥2 in 10 patients), 27 (79%) contained intra-aneurysmal thrombi, and in each, the thrombus severely narrowed the lumen. Additionally, atherosclerotic plaque was present in the aneurysmal wall in all 27 aneurysms containing thrombi and also in the major coronary arteries uninvolved by aneurysm. The causes of the aneurysms in the 16 patients with intra-aneurysmal thrombi were therefore considered atherosclerotic. In the other 4 patients, with 7 aneurysms, none contained intra-aneurysmal thrombus or atherosclerotic plaque, and the aneurysms were considered congenital. Clinical diagnosis of coronary aneurysm was not made in any of the 20 patients, but none had proper imaging studies during life. Despite the coronary aneurysms and the associated luminal narrowing, only 8 patients (40%) had left ventricular wall scarring or necrosis or clinical evidence of myocardial ischemia. Proper therapy remains ill defined.     

Qualitative and quantitative comparison of amounts of narrowing by atherosclerotic plaques in the major epicardial coronary arteries at necropsy in sudden coronary death, transmural acute myocardial infarction, transmural healed myocardial infarction and unstable angina pectoris

The amounts of narrowing of the 4 major (left main, left anterior descending, left circumflex and right) epicardial coronary arteries by atherosclerotic plaques were compared in 4 subsets of coronary patients. Of the 129 patients studied at necropsy, an average of 2.7 of the 4 arteries was narrowed greater than 75% in cross-sectional area at some point (0.7/4 in controls), and the group with unstable angina pectoris (3.2/4) had more narrowing than did the groups with sudden coronary death (2.8/4), acute myocardial infarction (2.7/4) and healed myocardial infarction (2.3/4). Each of the 4 major epicardial coronary arteries was divided into 5-mm long segments and a histologic section was prepared and stained by the Movat method of each of the 6,461 segments in the 129 patients and in the 1,849 segments in the 40 control subjects. In the 129 patients, 35% of the 5-mm segments were narrowed 75 to 100% in cross-sectional area (3% in controls) and the group with unstable angina had the highest percent (48%) of segments severely narrowed compared to the groups with sudden coronary death (36%), acute myocardial infarction (34%) and healed myocardial infarction (31%). Thus, of the 4 subsets of patients with fatal coronary artery disease studied at necropsy, those with unstable angina pectoris had the most severe and extensive coronary atherosclerosis.     

Amounts of coronary arterial narrowing by atherosclerotic plaques in clinically isolated mitral valve stenosis: Analysis of 76 necropsy patients older than 30 years

Although several studies have described the status of the coronary arteries by angiography in patients with mitral stenosis (MS), few necropsy studies of the coronary arteries in these patients are available. The present report describes in detail the amounts of narrowing by atherosclerotic plaque of the 4 major epicardial coronary arteries in 76 necropsy patients, aged 31 to 79 years (mean 53) with clinically isolated MS (with or without associated mitral regurgitation but without aortic valve dysfunction). Of the 76 patients, ≥1 major coronary artery was narrowed >75% in cross-sectional area (XSA) in 38 (50%) and in 10 of the 38 patients ≥1 major coronary artery was totally occluded or nearly so (>95% XSA narrowing). A higher percent of the 29 men had significant (>75% XSA) coronary narrowing than did the 47 women (62 vs 44%) and the men had more major coronary arteries significantly narrowed compared with the women (31 of 116 arteries [27%] vs 33 of 188 arteries [18%]). The 4 major coronary arteries in the 76 patients were divided into 5-mm segments and examined histologically: of the 3,124 segments (41 per patient), 620 segments (20%) were narrowed 0 to 25% in XSA, 1,826 (58%) were narrowed 26 to 50%, 470 (15%) were narrowed 51 to 75%, 188 (6%) were narrowed 76 to 95%, and 20 segments (1%) were narrowed 96 to 100% in XSA. The percent of segments narrowed >75% in XSA was 9% in the men and 5% in the women. The percent of segments narrowed >75% in XSA was highly variable in the 38 patients with significant narrowing, ranging from 2 to 59% (mean 13%). Grossly visible left ventricular scars were present in 11 patients and in each they involved the posterior (inferior) wall; 8 of the 11 patients had significant coronary narrowing and 3 did not. Angina pectoris was present in 13 patients, 8 (62%) had significant coronary narrowing and 5 (38%) did not.     

Coronary atherosclerosis in unheralded sudden coronary death under age 50: histo-pathologic comparison with 'healthy' subjects dying out of hospital

AIM: sudden coronary death (SCD) in older individuals is generally associated with extensive coronary atherosclerosis, although it may be the first manifestation of ischaemic heart disease. In younger age-groups, SCD may occur in the presence of less severe disease. We sought to (1) examine the extent of coronary atherosclerosis in young victims of SCD compared with age- and sex-matched controls, (2) analyse the composition of atherosclerotic plaques in these patients, (3) identify the predominant mechanism of SCD, and (4) evaluate the possibility of detecting this mechanism on the basis of morphologic plaque features, in particular presence and amount of lipid accumulation and calcific deposits. METHODS AND RESULTS: coronary arteries were obtained at autopsy from 28 victims of SCD under age 50 with no prior clinical manifestation of ischaemic heart disease (IHD) and no myocardial scar formation and from 16 age- and sex-matched subjects dying of noncardiac causes out of hospital. Sections of all available major coronary arteries were cut in 5-mm intervals to yield a total of 1357 histologic sections, which were analysed using digitised planimetry. Victims of SCD had significantly more major coronary arteries per subject with luminal area narrowing > or = 75% than controls (on average, 2.1 vs. 0.2). Plaque area per histologic section was 5.1 +/- 2.1 mm(2) in SCD cases and 2.0 +/- 0.9 mm(2) in controls (P < 0.001). The major constituent of all plaques was fibrous tissue. Lipid core area per section was 0.49 +/- 0.59 mm(2) in SCD cases and 0.004 +/- 0.01 mm(2) in controls (P < 0.001), and calcified plaque area was 0.18 +/- 0.19 mm(2) in SCD cases and 0.02 +/- 0.05 mm(2) in controls (P < 0.001), both defining significant differences between SCD cases and controls. Arterial thrombosis, most often with underlying plaque rupture was the mechanism of SCD in > 80% of the cases. Considering histologic sections with > or = 50 and with > or = 75% area stenosis, plaque rupture was independently predicted by lipid core area. Calcific deposits were a frequent feature of plaque rupture but were only associated with it in univariate analysis. CONCLUSIONS: the extent and severity of coronary atherosclerosis in young victims of SCD as the first manifestation of IHD was substantially greater than in age-and sex-matched controls and comparable with that previously reported in SCD cases with a broader age range. Lipid core and calcified plaque areas provided for excellent separation between the two groups, which may have implications for identifying persons at increased risk for SCD by non invasive visualisation and assessment of the coronary arteries.     

Quantification of coronary arterial narrowing and of left ventricular myocardial scarring in healed myocardial infarction with chronic,eventually fatal,congestive cardiac failure

A qualitative and quantitative analysis is described of the amount of ventricular wall myocardial scarring and the degree and extent of coronary arterial narrowing by atherosclerotic plaques in the entire lengths of each of the four major epicardial coronary arteries in 18 necropsy patients with healed transmural myocardial infarcts, and chronic, eventually fatal, congestive heart failure. In all 18 patients, the healed infarcts involved greater than 40 per cent of the left ventricular wall, all had very dilated right and left ventricular cavities, all had hearts weighing more than 450 g (average = 587 g), all had intractable congestive heart failure for longer than three months (average = 2.3 years), and half had intraventricular mural thrombi. Of 1,012 five millimeter segments of the four major epicardial coronary arteries examined in the 18 patients (average 54 segments per patient), 298 segments (29 per cent) were 76 to 100 per cent narrowed in cross-sectional area by atherosclerotic plaques (in 16 control subjects = 6 per cent), 370 (37 per cent) were 51 to 75 per cent narrowed (controls = 35 per cent), 227 (23 per cent) were 26 to 50 per cent narrowed (controls = 43 per cent), and 117 (11 per cent) were 0 to 25 per cent narrowed (controls = 16 per cent). The amount of severe (>75 per cent) narrowing of the right, left anterior descending and left circumflex coronary arteries was similar in the 18 study patients. The left main coronary artery was not severely narrowed in any patient. The amount of severe narrowing in the distal one half of the right, left anterior descending and left circumflex coronary arteries was similar to that in the proximal halves of these three arteries. The per cent of 5 mm segments of coronary artery narrowed 76 to 100 per cent in cross-sectional area in the nine patients was similar to that in the nine patients without left ventricular aneurysm.     

Degrees of coronary arterial narrowing at necropsy in men with large fusiform abdominal aortic aneurysm.

In 27 patients (mean age at death 72 +/- 9 years) with abdominal aortic aneurysm (AAA) > or = 5.0 cm in its widest transverse diameter, the amounts of narrowing at necropsy in the 4 major (left main, left anterior descending, left circumflex, and right) epicardial coronary arteries were determined. During life, 12 of the 27 patients (44%) had symptoms of myocardial ischemia: angina pectoris alone in 2, acute myocardial infarction alone in 3, angina pectoris and acute myocardial infarction in 5, and sudden coronary death in 2. Ten of the 27 patients (37%) died from consequences of myocardial ischemia. Six (22%) died from rupture of the AAA. Grossly visible left ventricular necrosis or fibrosis, or both, was present in 15 patients (56%). Of the 27 patients, 23 (85%) had narrowing 76 to 100% in cross-sectional area of 1 or more major coronary arteries by atherosclerotic plaque. The mean number of coronary arteries per patient severely (> 75%) narrowed was 2.0 +/- 1.3/4.0. Of the 108 major coronary arteries in the 27 patients, 55 (51%) were narrowed > 75% in cross-sectional area by plaque. The 4 major coronary arteries in the 27 patients were divided into 5-mm segments and a histologic section, stained by the Movat method, was prepared from each segment. The mean percentages of the resulting 1,475 five-mm segments narrowed in cross-sectional area 0 to 25%, 26 to 50%, 51 to 75%, 76 to 95% and 96 to 100% were 17, 37, 28, 15 and 3%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

The frequency and significance of coronary arterial thrombi and other observations in fatal acute myocardial infarction: a study of 107 necropsy patients

Observations made from histologie study of the entire extramural coronary arterial tree are described in 107 patients who died of acute ischemie heart disease: seventy-four had transmural left ventricular myocardial infarction, nine had necrosis limited to the inner one half of the left ventricular myocardium (acute subendocardial infarcts) and twenty-four died suddenly (less than six hours from onset of symptoms of myocardial ischemia) without histologically detectable myocardial necrosis. Old atherosclerotic plaquing was diffuse and extensive in the extramural coronary arteries in 104 of the 107 patients. The lumens of at least two of the three major extramural coronary arteries (right, left anterior descending and left circumflex) were narrowed more than 75 per cent by old atherosclerotic plaques in 101 of the 107 patients.Coronary arterial thrombi were found in forty (54 per cent) of the seventy-four patients with transmural necrosis, in none of the nine with only subendocardial necrosis and in two (8 per cent) of the twenty-four who died suddenly. In thirty-seven of the forty-two patients with antemortem coronary arterial clots the lumen of the vessel containing the thrombus was already narrowed more than 75 per cent by old atherosclerotic plaques at or distal to the thrombus. The infrequency of coronary thrombi in patients who died of acute cardiovascular collapse without myocardial necrosis, in those in whom necrosis was limited to the subendocardium, in those who died without cardiogenic shock or congestive cardiac failure, and their occurrence at, or proximal to, sites already severely narrowed by old atherosclerotic plaques suggest that coronary thrombi are consequences rather than causes of acute myocardial infarction. The occurrence of components of thrombi, i.e., fibrin and platelets, in old atherosclerotic plaques and the finding of components of old atherosclerotic plaques, i.e., foam cells, cholesterol clefts, pultaceous debris and calcific deposits, in known thrombi (for example, those located in the left atrium of patients with mitral stenosis) strongly suggest, however, that old atherosclerotic plaques are derived, at least in part, from organization of thrombi.     

Amounts of coronary arterial narrowing by atherosclerotic plaques in clinically isolated,chronic, pure aortic regurgitation: Analysis of 37 necropsy patients older than 30 years

The degree of cross-sectional area (XSA) narrowing by atherosclerotic plaque in each of the 4 major epicardial coronary arteries (right, left main, left anterior descending and left circumflex) was determined at necropsy in 37 patients (30 men and 7 women) aged 34 to 77 years (mean 54) with severe, isolated, chronic, pure aortic regurgitation (AR). In 7 patients (19%), ≥ 1 major coronary artery was narrowed 76 to 100% in XSA at some point. Of the 148 major coronary arteries examined in the 37 patients, 12 arteries (8% ) were narrowed at some point 76 to 100% in XSA. Each of the 148 major coronary arteries were divided into 5-mm-long segments (average 53 per patient) and a histologic section from each segment was examined. Of the 1,977 segments, 1,087 were narrowed 0 to 25%, 669 (34%) 26 to 50%, 170 (9%) 51 to 75%, 48 (2%) 76 to 95% and 3 (0.001%) 96 to 100%. The average amount of XSA narrowing by atherosclerotic plaque per segment was about 28%. Of the 37 patients, 9 had had angina pectoris, 2 of whom had significant (> 75% XSA reduction) coronary narrowing; 2 other patients had had acute myocardial infarction clinically, 1 of whom had significant coronary narrowing at necropsy. Thus, in general, the amount of coronary narrowing in our 37 adults with severe, pure, isolated, chronic AR was relatively mild.     

Histopathology of the conduction system in sudden death from coronary heart disease.

Sudden cardiac death (SCD) has been attributed to the development of lethal dysrhythmias in coronary heart disease victims, and several recent autopsy surveys showed that 10 to 50% of SCD patients had unsuspected acute myocardial infarction (AMI). The present study concerned histopathological findings of the conduction system in 49 SCD (within six hours of the onset of acute symptoms) patients; 39 with established AMI (group A) and ten without (group B). Both groups showed high incidence of cardiomegaly, significant coronary artery disease affecting one or more vessels, and acute myocardial ischemia detectable by specific histological criteria. Stenosis of nutrient vessels of the conduction system was present in about 50% of the atrioventricular (A-V) node arteries and about 25% of the sinoatrial (SA) node arteries in both groups of SCD patients. Nonspecific "degenerative" changes (fibrosis, fatty infiltration, or both) of the conduction tissue, which might or might not represent results of old ischemic injury, also occurred with similar frequencies. Acute changes (infarction, hemorrhage) of the A-V node and bundle branches were found only in two group A patients, both had massive septal infarction. Thus, the conduction tissue appeared more resistant to ischemic injury and was overtly damaged only on rare occasions in fatal AMI. The scarcity of acute lesions in the conduction system itself suggested that lethal dysrhythmia in SCD was probably due to electrical instability of the acutely ischemic contractile myocardium rather than a direct injury to the specialized tissue of the heart.